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The objective of this project is to study the proteome in different tissues of huntingtin knock-in allelic series in mice. In the current part of the study, hippocampus samples from the complete remaining allelic series collected at 2, 6, and 10 months were analyzed. To this end, comprehensive quant...
ORGANISM(S): Mus musculus (Mouse) 
2017-03-23 | PXD005538 | Pride
The objective of this project is to study the proteome in different tissues of huntingtin knock-in allelic series in mice. In the current part of the study, cerebellum samples from the complete remaining allelic series collected at 2, 6, and 10 months were analyzed. To this end, comprehensive quanti...
ORGANISM(S): Mus musculus (Mouse) 
2017-03-23 | PXD005526 | Pride
The objective of this project is to study the proteome in different tissues of huntingtin knock-in allelic series in mice. In the current part of the study, striatum samples from the complete remaining allelic series collected at 2, 6, and 10 months were analyzed. To this end, comprehensive quantita...
ORGANISM(S): Mus musculus (Mouse) 
2017-05-26 | PXD006302 | Pride
The objective of this project is to study the proteome in different tissues of huntingtin knock-in allelic series in mice. In the current part of the study, liver samples from the complete remaining allelic series collected at 2, 6, and 10 months were analyzed. To this end, comprehensive quantitativ...
ORGANISM(S): Mus musculus (Mouse) 
2017-03-22 | PXD005641 | Pride
Constitutively activating internal tandem duplication (ITD) alterations of the receptor tyrosine kinase FLT3 (Fms-like tyrosine kinase 3) are common in acute myeloid leukemia (AML) and classifies FLT3 as an attractive therapeutic target. So far, application of FLT3 small molecule inhibitors such as ...
ORGANISM(S): Homo sapiens (Human) 
2017-05-02 | PXD004442 | Pride
Treatment with inhibitors of the receptor tyrosine kinase FLT3 are currently studied as promising therapies in acute myeloid leukemia (AML). However, only a subset of patients benefit from these treatments and the presence of activating mutations within FLT3 can predict response to a certain extent ...
ORGANISM(S): Homo sapiens (Human) 
2017-05-10 | PXD006475 | Pride
To gain insight into how mutant Huntingtin (mHTT) CAG repeat length may modify Huntington’s disease (HD) pathogenesis, we profiled mRNA in over 600 brain and peripheral tissue samples from HD knock-in mice with increasing CAG repeat length. We find repeat length dependent transcriptional signatures ...
ORGANISM(S): Mus musculus (Mouse) 
2016-02-16 | PXD003442 | Pride
The objective of this project is to study the proteome in different tissues of huntingtin knock-in allelic series in mice. In the current part of the study, heart samples from the complete allelic series collected at 2, 6, and 10 months were analyzed. To this end, comprehensive quantitative, label-f...
ORGANISM(S): Mus musculus (Mouse) 
2018-09-03 | PXD010958 | Pride
The objective of this project is to study the proteome in different tissues of huntingtin knock-in allelic series in mice. In the current part of the study, gastrocnemius samples from the complete remaining allelic series collected at 2, 6, and 10 months were analyzed. To this end, comprehensive qua...
ORGANISM(S): Mus musculus (Mouse) 
2018-09-03 | PXD010957 | Pride
Animal models play a critical role in the study of Huntington’s disease (HD), for example to elucidate underlying molecular mechanisms or to develop novel therapeutic venues. One of the first transgenic mouse models of HD, the R6/2 line, has been described in 1996 and has since become one of the mos...
ORGANISM(S): Mus musculus (Mouse) 
2019-06-03 | PXD013771 | Pride
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